Catherine Hume, Nancy Sabatier and John Menzies
Endocrinology (in press)
Oxytocin is a potent anorexigen and is believed to have a role in satiety signalling. We developed rat models to study the activity of oxytocin neurones in response to voluntary consumption or oral gavage of foods using c-Fos immunohistochemistry and in vivo electrophysiology.
Using c-Fos expression as an indirect marker of neural activation, we showed that the percentage of magnocellular oxytocin neurones expressing c-Fos increased with voluntary consumption of sweetened condensed milk (SCM). To model the effect of food in the stomach, we gavaged anaesthetised rats with SCM. The percentage of supraoptic nucleus and paraventricular nucleus magnocellular oxytocin-immunoreactive neurones expressing c-Fos increased with SCM gavage but not with gastric distention. To further examine the activity of the supraoptic nucleus, we made in vivo electrophysiological recordings from SON neurones while anaesthetised rats were gavaged with SCM or single cream. Pharmacologically identified oxytocin neurones responded to SCM gavage with a linear, proportional and sustained increase in firing rate but cream gavage resulted in a transient reduction in firing rate. Blood glucose increased after SCM gavage but not cream gavage. Plasma osmolarity and plasma sodium were unchanged throughout.
We show that in response to a high-sugar, but not high-fat, food in the stomach, there is an increase in the activity of oxytocin neurones. This does not appear to be a consequence of stomach distention or changes in osmotic pressure. Our data suggest that the presence of specific foods with different macronutrient profiles in the stomach differentially regulates the activity of oxytocin neurones.